These findings, derived from a large sample of unmedicated depressed outpatients, indicate that major depressive disorder in healthy younger ambulatory adults does not cause appreciable impairments in cognitive functioning in the absence of clinical and course-of-illness features.

Objective-Heightened amygdala reactivity to aversive stimuli in major depression is regarded as a core feature of the underlying physiology but individual differences in amygdala response may also arise secondary to persistent changes in limbic function during early neurodevelopment relative to stressors such as childhood trauma. We sought to determine whether heightened amygdala response is a core feature of depression or a general risk factor for psychopathology secondary to early life stress.Method-Twenty unipolar depressed patients with and without a history of significant early life trauma and 16 healthy comparison subjects underwent functional MRI in a cross-sectional study comparing neural response to sad and neutral faces.Results-We observed a robust positive correlation between physical abuse and right amygdala response. A much weaker relationship with other forms of abuse and neglect was also found, suggesting differences between abuse subtypes and amygdala response. Group differences in amygdala response suggest heightened reactivity was not characteristic of persons with depression in general but was true primarily in those with a significant history of abuse.Conclusion-These findings suggest the relationship between childhood trauma and risk for depression is mediated by heightened amygdala response but varies by abuse type. Preliminary evidence for two distinct depression phenotypes based on trauma history was also supported, consistent with differential etiology.Keywords childhood trauma; amygdala; stress sensitization; depression Major depressive disorder is a serious illness estimated to affect 13 to 14 million adults annually and approximately 16% of the U.S. population across the lifespan (Kessler et al., 2003). Furthermore, the considerable social, occupational and workplace related costs associated with impaired function are estimated in the tens of billions of dollars each year (Wang et al., 2006). Childhood maltreatment has emerged as a significant risk factor for the onset of adult depression with over 500,000 documented cases of physical and sexual abuse © 2010 Elsevier Ltd. All rights reserved. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. (Sedlak et al., 2010). Despite the widely appreciated magnitude of the problem, the precise mechanism by which childhood trauma may increase the risk for depression remains unclear. NIH Public AccessExaggerated amygdala response is regarded as a core feature of the underlying physiology of unipolar depression (Price and Drevets, 2010). Imaging studies utilizing both positron emission tomography (PET)...

BackgroundPrior studies have independently reported associations between major depressive disorder (MDD), elevated cortisol concentrations, early adverse events and region-specific decreases in grey matter volume, but the relationships among these variables are unclear. In the present study, we sought to evaluate the relationships between grey matter volume, early adverse events and cortisol levels in MDD.Methods/ResultsGrey matter volume was compared between 19 controls and 19 individuals with MDD using voxel-based morphometry. A history of early adverse events was assessed using the Childhood Trauma Questionnaire. Subjects also provided salivary cortisol samples. Depressed patients showed decreased grey matter volume in the rostral ACC as compared to controls. Rostral ACC volume was inversely correlated with both cortisol and early adverse events.ConclusionsThese findings suggest a key relationship between ACC morphology, a history of early adverse events and circulating cortisol in the pathophysiology of MDD.

Previous research on chronic depression has focused on its link with other mood disorders and Axis II personality disorders. However, there are few data examining whether the cognitive perspective applies to this condition. In this cross-sectional study, 42 outpatients with chronic depression were compared with 27 outpatients with nonchronic major depressive disorder and 24 never psychiatrically ill controls on cognitive variables thought to be related to vulnerability to depression (e.g., dysfunctional attitudes, attributional style, a ruminative response style, and maladaptive core beliefs). Both depressed groups were more elevated than a never-ill comparison group. However, chronically depressed individuals were generally more elevated on measures of cognitive variables than those with major depressive disorders even after controlling for mood state and personality disorder symptoms.

The present study examined whether training in cognitive coping skills would enhance pain coping strategies and alter pain perception in adults with sickle cell disease (SCD). Sixty-four African Americans with SCD were randomly assigned to either a cognitive coping skills condition (three 45-min sessions in which patients were trained to use 6 cognitive coping strategies) or a disease-education control condition (three 45-min didactic-discussion sessions about SCD). Pain sensitivity to calibrated noxious stimulation was measured at pre- and posttesting, as were cognitive coping strategies, clinical pain, and health behaviors. Results indicated that, compared with the randomly assigned control condition, brief training in cognitive coping skills resulted in increased coping attempts, decreased negative thinking, and lower tendency to report pain during laboratory-induced noxious stimulation.

The purpose of the current study was to investigate depression and health care use in patients with sickle cell disease (SCD). Forty-four adults with SCD were interviewed and data from 43 participants, both with (n = 11) and without (n = 32) depression, were used for further analyses. Data from one potential subject were excluded on the basis of diagnosis. The full evaluation included the Structured Clinical Interview for DSM-III-R Disorders (SCID) and the Center for Epidemiologic Studies--Depression Scale (CES-D), as well as measures of psychosocial and behavioral functioning. Good between-instrument agreement was found between the self-report and interview-based measures of depression. However, the functioning data did not entirely support the use of a more stringent cutoff score on the CES-D. Findings suggest that the purpose of the evaluation should be factored into the decision-making process when determining which cutoff score should be utilized (i.e. what is the cost-benefit ratio for false-positives vs. false-negatives). A series of hierarchical regression analyses supported the finding that disease severity alone does not explain the level of functioning displayed by patients. More importantly, the patient's perceived functioning was the best indicator of health care use within a 1-year period. Furthermore, specific interventions that target negative thinking and distorted cognitions, as well as provide psychoeducation, such as cognitive-behavioral therapy, need to be further explored within this population.

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Failure of the circuit implicated in emotion regulation was associated with a significant history of ELT but not with MDD more broadly. Non-ELT related depression was associated with intact regulation of emotion despite the absence of difference in severity of illness. These findings indicate opposing system-level differences within depression relative to ELT are expressed as differential amygdala reactivity.